Ceramide in Suicidal Death of Erythrocytes

被引:193
作者
Lang, Florian [1 ]
Gulbins, Erich [2 ]
Lang, Philipp A.
Zappulla, Donatella [3 ,4 ]
Foeller, Michael
机构
[1] Univ Tubingen, Inst Physiol, Dept Physiol, D-72076 Tubingen, Germany
[2] Univ Duisburg Essen, Dept Mol Biol, Essen, Germany
[3] Univ Catania, Sch Med, Inst Physiol, Catania, Italy
[4] Univ Catania, Sch Med, Dept Internal Med, Catania, Italy
关键词
Apoptosis; Red blood cells; Anemia; Sepsis; Malaria; PROGRAMMED CELL-DEATH; RED-BLOOD-CELLS; MEMBRANE PHOSPHOLIPID ASYMMETRY; PHOSPHATIDYLSERINE EXPOSURE; CATION CHANNELS; PLASMODIUM-FALCIPARUM; ENHANCED SUSCEPTIBILITY; BETA-THALASSEMIA; CA2+ ENTRY; STIMULATION;
D O I
10.1159/000315102
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The suicidal death of erythrocytes or eryptosis is characterized by cell shrinkage, membrane blebbing and cell membrane phospholipid scrambling resulting in phosphatidylserine exposure at the cell surface. Eryptosis is stimulated in a wide variety of diseases including sepsis, haemolytic uremic syndrome, malaria, sickle-cell anemia, beta-thalassemia, glucose-6-phosphate dehydrogenase (G6PD)-deficiency, phosphate depletion, iron deficiency and Wilson's disease. Moreover, eryptosis is elicited by osmotic shock, oxidative stress, energy depletion as well as a wide variety of endogenous mediators and xenobiotics. Excessive eryptosis is observed in erythrocytes lacking the cGMP-dependent protein kinase type I (cGKI) or the AMP-activated protein kinase AMPK. Inhibitors of eryptosis include erythropoietin, nitric oxide NO, catecholamines and high concentrations of urea. Eryptosis-triggering diseases and chemicals are partially effective by stimulating the formation of ceramide, which in turn fosters cell membrane scrambling. Accordingly, ceramide-induced eryptosis participates in the pathophysiology of several diseases and contributes to the effects of a large number of xenobiotics. The mechanisms underlying ceramide formation in erythrocytes are, however, still ill defined. In case of osmotic cell shrinkage, ceramide formation is apparently due to activation of phospholipase 2, leading to formation of platelet activating factor PAF and PAF-dependent stimulation of ceramide formation, which possibly involves acid sphingomyelinase. Additional experiments are needed to conclusively define the ceramide-generating enzyme and the ceramide-dependent cellular events eventually leading to suicidal erythrocyte death. Copyright (C) 2010 S. Karger AG, Basel
引用
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页码:21 / 28
页数:8
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